Abstract
Background Reduction of post-contrast T1 in remote normal myocardium was recently reported in patients with AMI, indicating that extracellular matrix expansion occurs in remote myocardium early after MI. Such extracellular matrix expansion observed in non-infarcted myocardium without edema seems to be one of key factors causing LV remodeling after MI. However, since the previous study only determined post-contrast T1, alteration of extracellular volume fraction (ECV) in remote myocardium early after MI is not investigated quantitatively. Consequently, we sought to quantify ECV in remote normal myocardium in AMI patients using T1 mapping before and after gadolinium contrast with hematocrit and heart-rate corrections, and investigate the association between ECV expansion in remote normal myocardium and extents of infarction and area at risk. Methods
Highlights
Reduction of post-contrast T1 in remote normal myocardium was recently reported in patients with AMI, indicating that extracellular matrix expansion occurs in remote myocardium early after MI
Both extracellular volume fraction (ECV) and native T1 were strongly associated with age in control subjects (y = 0.12x+18.16, r = 0.689, p = 0.003 and y = 1.5175x+1202.6, r = 0.503, p = 0.047, respectively)
Age-corrected remote myocardial ECV was significantly larger in AMI patients (28.8 ± 2.4%) than in normal subjects (26.0 ± 1.4%, p = 0.0196), whereas age-corrected native remote myocardial T1 was significantly longer in AMI patients (1349 ± 47 ms) than in control subjects (1294 ± 30 ms, p = 0.0058)
Summary
Reduction of post-contrast T1 in remote normal myocardium was recently reported in patients with AMI, indicating that extracellular matrix expansion occurs in remote myocardium early after MI. Such extracellular matrix expansion observed in non-infarcted myocardium without edema seems to be one of key factors causing LV remodeling after MI. We sought to quantify ECV in remote normal myocardium in AMI patients using T1 mapping before and after gadolinium contrast with hematocrit and heart-rate corrections, and investigate the association between ECV expansion in remote normal myocardium and extents of infarction and area at risk
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